Pseudechis australis

   1.1 Scientific Name
   1.2 Family
   1.3 Common Names
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
   2.5 Venom apparatus, poisonous parts or organs
   2.6 Main toxins
   3.1 Description of the animal
      3.1.1 Special identification features
      3.1.2 Habitat
      3.1.3 Distribution
   3.2 Poisonous/venomous Parts
   3.3 The toxin(s)
      3.3.1 Name
      3.3.2 Description
   3.4 Other chemical contents
   4.1 Uses
   4.2 High risk circumstances
   4.3 High risk geographical areas
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
      5.5.1 Bites
      5.5.2 Stings
   5.6 Others
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination by route of exposure
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data Adults Children
      7.2.2 Relevant animal data
      7.2.3 Relevant in vitro data
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses
      8.1.2 Storage of laboratory samples and specimens Toxicological analyses
      8.1.3 Transport of laboratory samples and specimens Toxicological analyses
   8.2 Toxicological analyses and their interpretation
      8.2.1 Tests on toxic ingredient(s) of materials Simple qualitative test(s) Advanced qualitative confirmation test(s) Simple quantitative method(s) Advanced quantitative method(s)
      8.2.2 Tests for biologicals specimens Simple qualitative test(s) Advanced qualitative confirmation test(s) Simple quantitative method(s) Advanced quantitative methods(s) Other dedicated methods(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical Investigations and Their Interpretation:
      8.3.1 Biochemical analyses Blood, plasma or serum Urine Other biological specimens
      8.3.2 Arterial blood gas analysis
      8.3.3 Haematological analyses
      8.3.4 Other (unspecified) analyses
      8.3.5 Interpretation of biomedical investigations
   8.4 Other Biomedical Investigations and Their Interpretation
   8.5 Summary of most essential biomedical and toxicological analyses
   9.1 Acute poisoning/envenomation
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning by:
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin exposure
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systematic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological CNS Peripheral nervous system Autonomic Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary Renal Other
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ear, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic Acid base disturbances Fluid and electrolyte disturbances Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Others
   10.1 General Principles
   10.2 Relevant laboratory analysis and other investigations
      10.2.1 Sample collection
      10.2.2 Biomedical analysis
      10.2.3 Toxicological analysis
      10.2.4 Other investigations.
   10.3 Life supportive procedures and symptomatic treatment
   10.4 Decontamination
   10.5 Elimination
   10.6 Antidote/antivenin treatment
      10.6.1 Adults
      10.6.2 Children
   10.7 Management discussion
   11.1 Case reports from literature
   11.2 Internally extracted data on cases
   11.3 Internal cases
   12.1 Availability of antidotes and antitoxins
   12.2 Specific preventative measures:
   12.3 Other
   13.1 Clinical and Toxicological
   13.2 Zoological
    1.   NAME

     1.1  Scientific Name

          Pseudechis australis

          (Cogger 1975, 1987; Cogger et al 1983; Covacevich 1988; 

     1.2  Family


          Genus: Pseudechis

     1.3  Common Names

          Scientific Name           Common Name

          Pseudechis australis      mulga snake, king brown
                     butleri        Butler's snake
                     colletti       Collett's snake
                     guttatus       spotted black snake,
                                    blue bellied black snake
                     papuanus       Papuan black snake
                     porphyriacus   red bellied black snake

    2.   SUMMARY

     2.1  Main risks and target organs

          Black snakes are only a moderately common cause of significant 
          snakebites in Australia. Severity depends on species, with P. 
          australis often causing significant envenomation while some other 
          species, notably P. porphyriacus, only rarely causing severe 
          envenomation. In the past P. papuanus has been thought to be a 
          significant cause of snakebites in Papua New Guinea, but there is 
          some doubt that this is still so. 
          Main risks are:  rhabdomyolysis, acute renal failure, and 
          possibly coagulopathy and neurotoxic paralysis in some species. 
          Target organs:  skeletal muscle, coagulation system, and possibly 
          the neuromuscular junction for some species. 

     2.2  Summary of clinical effects

          Locally: usually immediately painful, with subsequent development 

          of mild to marked local oedema, and sometimes ecchymosis. Bite 
          marks vary from single puncture, through multiple punctures, to 
          multiple scratches. Local secondary infection unusual. Venom may 
          spread to draining lymph nodes with consequent pain, tenderness 
          or swelling.
          Systemic: headache, nausea, vomiting, abdominal pain, impaired 
          consciousness, occasionally loss of consciousness  and possibly 
          convulsions. Coagulopathy with overt bleeding manifestations is 
          rare. Neurotoxic paralysis is not well documented clinically. 
          Muscle movement is painful. Acute renal failure. Rhabdomyolysis 
          may dominate the clinical picture for P. australis bites and 
          possibly for P. butleri bites. 

     2.3  Diagnosis

          Monitor coagulation to establish the presence and extent of 
          coagulopathy. This should be performed at presentation, on 
          development of symptoms or signs of systemic envenomation, and 1-
          2 hours after antivenom therapy. However, coagulopathy due to 
          Pseudechis bites is poorly documented and defibrination has not 
          been reported.
          In the absence of a haematology laboratory, whole blood clotting 
          time in a  glass test tube is useful. If a laboratory is 
          available, prothrombin ratio, activated partial  thromboplastin 
          time, thrombin clotting  time, fibrinogen level, and fibrin(ogen) 
          breakdown products are most useful.
          Other useful tests are complete blood picture and platelet count, 
          serum electrolytes, creatinine, urea, serum enzymes, especially 
          creatine kinase, urine output and urine myoglobin, and venom 
          detection using CSL Venom Detection Kit. Best sample for venom 
          detection is a swab from the bite site (sample swab stick in 
          kit). If patient  has systemic envenomation, urine may also be 
          useful sample. Blood is not a reliable sample. 

     2.4  First-aid measures and management principles

          (a)   If the patient develops evidence of respiratory or cardiac 
                failure, use standard cardiopulmonary resuscitation 
                techniques to maintain life. 
          (b)   The patient should be encouraged to lie still, and 
                reassured to avoid panic. 
          (c)   A broad compression bandage should  be applied over the 
                bitten area, at about the same pressure as for a sprained 
                ankle.  This bandage should then be extended distally, then 
                proximally, to cover as much of the bitten limb as 
          (d)   The bandaged limb should be firmly immobilised using a 
          (e)   The bite site wound should not be washed, cleaned, cut, 

                sucked, or treated with any substance. 
          (f)   Tourniquets should not be used.
          (g)   The patient  should be  transported to appropriate medical 
          (h)   Nil orally unless the patient will not reach medical care 
                for a prolonged period of time, in which case only water 
                should be given by mouth. No food should be consumed. 
                Alcohol should not be used. 
          (i)   If the offending snake has been killed it should be brought 
                with the patient for identification. 
          (j)   Remove any rings, bangles etc from the bitten limb.
          Treatment principles
          (a)   Specific: If the patient has systemic envenomation, give 
                specific snake antivenom (CSL). 
                Snake                    Antivenom  
                Pseudechis australis     black snake antivenom
                           butleri       black snake antivenom
                           colletti      tiger snake antivenom 
                           guttatus      tiger snake antivenom
                           porphyriacus  tiger snake antivenom
                           papuanus      black snake antivenom
          (b)   General:  Support  of  cardiac  and  respiratory  
                functions; treatment of  shock;  maintenance  of  adequate  
                fluid  load, electrolyte balance, and  renal output; 
                tetanus  prophylaxis; treatment of local sepsis  with  
                antibiotics;  treatment  of significant blood loss with 
                blood transfusion. 
          (c)   Local: Do not clean or touch the local wound until 
                appropriate samples taken for  venom detection. Thereafter 
                ensure antisepsis. Early surgical intervention is generally 
                contraindicated, and is only rarely indicated in the late 
                stages if significant local necrosis has developed. 

     2.5  Venom apparatus, poisonous parts or organs

          Venom is produced in paired modified salivary glands, 
          superficially situated beneath the scales, posterior to the eye, 
          and surrounded by muscles, the contraction of which compress the 
          glands, expelling venom anteriorly via venom ducts to the fangs. 
          The fangs are likewise paired, situated at the anterior part of 
          the upper jaw, on the maxillary bones. They have an enclosed 
          groove for venom transport, with an exit point near the fang tip.

     2.6  Main toxins

          Pseudechis  venom  is  a  complex  mixture  of  protein and non-
          protein components, not all of which have been fully evaluated. 
          (a)   Neurotoxins:  both presynaptic  and postsynaptic may be 
                present, though neither appear to be clinically important 
                in human envenomation. 
          (b)   Procoagulants:  principally  anticoagulants.
          (c)   Myotoxins:   second  action  of  presynaptic  neurotoxins  
                which is a phospholipase A2, and also a separate action of 
                distinct phospholipase toxins without significant 
                neurotoxic action. 


     3.1  Description of the animal

          3.1.1 Special identification features

          The black snakes belong to the Class Reptilia; Order Squamata; 
          Suborder Serpentes: Family Elapidae.  They are oviparous (except 
          P. porphyriacus which is ovoviviparous),  diurnal or crepuscular, 
          and in warm weather may be nocturnal.  Food varies with species, 
          subspecies and locality, and includes frogs, small lizards, and 
          small mammals. 
          Black snake dentition is proteroglyphous (maxilla), the paired  
          fangs being situated in the anterior  portion  of  the  upper  
          jaw  ("front fanged"), on partly mobile  maxillae allowing  
          limited elevation for strike .  The  fangs have venom transport  
          grooves, enclosed for most of their length. For fang details see 
          section 3.3.2. 
          Six species are currently recognized.
                Scientific Name           Common Name
                Pseudechisaustralis       mulga snake, king brown
                          butleri         Butler's snake
                          colletti        Collett's snake
                          guttatus        spotted black snake, 
                                          blue bellied black snake
                          papuanus        Papuan black snake
                          porphyriacus    red bellied black snake 
                Genus Pseudechis:  Characterized by smooth scales, mid-body 
                scales in 17-19 rows, anal and subcaudal scales variable, 
                anal usually divided, but anterior subcaudals usually 
                single, suboculars absent, head usually broad to triangular 
                in outline with some vertical compression. 

                P. australis
                Scalation:  smooth, 17 rows in mid body, ventrals 185-225, 
                anal divided (occasionally single), subcaudals 50-75, 
                usually single anteriorly. 
                Length:   2 metres (max over 2.7 m)
                Colour:  Colour usually uniform dorsally, ranging from pale 
                brown, through russet brown, to dark brown depending on 
                specimen and location. Scales usually lighter in colour 
                proximally becoming darker near their tips giving an 
                overall reticulated pattern on close inspection. Ventrally 
                cream to pink often with darker blotches. 
                P. butleri
                Scalation:  smooth, 17 rows in mid body, ventrals 204-216, 
                anal usually divided, subcaudals 55-65, usually single 
                Length:   1.6 metres
                Colour:  Sides and front of head brown or reddish brown, 
                rest of head dorsally black or brown black, extending to 
                nape of neck, body with reticulated appearance as each 
                scale has a base colour of dark brown to black with a large 
                central area of pale yellow. Ventrally yellow with black 
                P. colletti
                Scalation:  smooth, 19 rows in mid body, ventrals 215-235, 
                anal usually divided, subcaudals 50-70, single anteriorly. 
                Length:  1.5 metres (maximum about 2 m).
                Colour:  Distinctive, with deep brown to black dorsally 
                with numerous irregular cross bands of pink, or cream 
                scales, tending to dominance laterally, more vivid in 
                juveniles where the colour may be deeper  and even orange 
                or red orange, ventrally cream to yellow or orange. 
                P. guttatus
                Scalation:  smooth, 19 rows in mid body, ventrals 175-205, 
                anal usually divided, subcaudals 45-65, single anteriorly. 
                Length:  1.5 metres (maximum about 2 m).
                Colour:  Variable. Two basic forms, one black to blue black 
                dorsally with grey to black ventrally (blue bellied black 
                snake), the other black with brown blotches dorsally and 
                laterally, grey ventrally (spotted black snake), and in 
                some specimens the dominant dorsal scale colour may be 

                cream with black tips. 
                P. papuanus
                Scalation:  smooth, 19-21 rows in mid body, ventrals 215-
                230, anal usually divided, subcaudals 45-65, mostly single 
                but divided posteriorly. 
                Length:  2.1 metres.
                Colour:  Dorsally black (occasionally brown), ventrally 
                grey or bluish grey. 
                P. porphyriacus
                Scalation:  smooth, 17 rows in mid body, ventrals 170-215, 
                anal usually divided, subcaudals 40-70, single anteriorly. 
                Length:  1.25 metres (maximum about 2.5 m).
                Colour:  Dorsally black, ventrally usually red, 
                occasionally pink, or pale cream to white, or black. 
                (Cogger 1971, Cogger 1975, Mirtschin & Davis 1983, Smith 

          3.1.2 Habitat

                Habitat varies with species ranging from arid lands to 
                Pseudechis australis (mulga snake, king brown)
                Found in a diverse range of habitats from arid areas across 
                central Australia, through to sub-tropical and tropical 
                regions. Principally diurnal, it is however active on warm 
                P.butleri (Butler's snake)
                Essentially similar to P. australis but with a more limited 
                range, not encompassing tropical areas. 
                P. colletti (Collett's snake)
                Relatively little known about the ecology of this snake, 
                but it is found principally in arid and semi-arid areas. 
                P. guttatus (Spotted black snake, blue bellied black snake)
                This species favours wetland areas including riverine and 
                floodplain habitats. 
                P. papuanus (Papuan black snake)

                The papuan black snake is confined to Papua New Guinea 
                chiefly in southern and coastal regions. It has been 
                recorded in savanna woodland, adjacent forrest, and in 
                swampland. The true distribution and ecology and habitat 
                preferences of this snake have yet to be defined. 
                P. porphyriacus (Red bellied black snake)
                Essentially a wetlands species favouring swamps, riverine, 
                and similar habitats. 

          3.1.3 Distribution

                The distribution for each species based on museum records 
                and published accounts is shown in Figures. 

     3.2  Poisonous/venomous Parts

          Venom glands (paired) situated superficially in posterior part of 
          head, connected by ducts to forward placed (paired) fangs.  Fangs 
          small, may leave classic single or double puncture in man, or a 
          more complicated array of scratches and other punctures, the 
          latter by non-fang teeth (White 1987a,c).  The classic bite mark 
          in plaster is shown in Figure. 

     3.3 The toxin(s)

          3.3.1 Name  

                P. australis   Mulga snake venom
                               Mulgatoxin a (specific myotoxin)
                               Pa 10a, Pa 11, Pa 13 (PLA2 [=phospholipase 
                               A2] toxins)
                P. porhyriacus Black snake venom
                               Pseudexin A,B,C (PLA2 toxins)
                P. colletti    Colletts snake venom
                P. guttatus    Spotted black snake venom
                P. papuanus    Papuan black snake venom

          3.3.2 Description

         Whole venom production based on milking specimens, usually 
            in captivity.  (White 1987b, Fairley & SPLATT, 1929) 
                Venom yield and fang length, where known, are listed below 
                (Fairley 1929b, Kellaway 1929, Kellaway and Thompson 1930, 
                Martin and Smith 1892, Sutherland 1983, White 1987a, 
                Worrell 1970, Morrison et al 1982) 

    Snake:         P.aus   P.but   P.col   P.gut   P.por   P.pap 
    Average adult
    fang length
    (mm)               6.5      -       -      3.5     4.0      -
    Average distance
    between fangs
    (mm)                -       -       -       -      12       -
    Average venom
    yield (mg)         180      -       30      -      40       -
    Maximum venom
    yield (mg)         600      -       50      -      94       -
    Mean venom injected
    (defensive strike)
    (mg)               61.6     -        -      -      1.3      -
    Mean venom left
    on skin
    (mg)               0.07     -        -      -      0.9      -
                Venom components
                Mulgatoxin a
                From P. australis venom: (also as Pa VIIIa,), Basic PLA2 
                single chain protein, 122 AA, 7 disulphide bridges, MW 
                13484 D, LD50 200 mg/kg ip mice, a specific myotoxin in 
                mice causing myoglobinuria, affecting skeletal muscle, and 
                with death due to probable paralysis at high doses, without 
                histological evidence of damage to heart or smooth muscle 
                (Leonardi et al 1979, Mebs & Samejima 1980) 
                P. a.Frac.5
                From P. australis venom: Lethal, causes myoglobinuria in 
                mice, LD50 0.25 mg/kg ip mice. (Leonardi et al 1979) 
                From P. porphyriacus venom: Initially described as a PLA 
                single chain polypeptide, MW 16500 D, LD50 0.48 mg/kg ip 
                mice. Later shown to be a dimer, then a mixture of 3 
                isomers, A,B,& C,with respective LD50s and MWs of; A= LD50 
                1.3 mg/kg ip mice, 117 AA, MW 13096D; B= LD50 0.75 mg/kg, 
                117 AA, MW 13002D; C= non-toxic in mice, not further 
                elaborated. It was further noted that monoclonal antibody 
                to Pseudexin neutralized the presynaptic neurotoxin from 
                tiger snake venom (notexin, Notechis scutatus). Although 

                principally described as a lethal myotoxin, it is therefore 
                possible that pseudexin also functions as a neurotoxin. 
                (Vaughan et al 1981, Moon & Rys 1984, Schmidt & Middlebrook 
                P. porph.Ib
                From P. porphyriacus venom: A lethal myotoxin, basic PLA2 
                protein, 120 AA, MW 13400D, LD50 6.4 mg/kg sc mice, minimum 
                dose for myoglobinuria 1.4 mg/kg sc mice. (Mebs & Samejima 
                P. coll/gut.
                From a mixture of P.  colletti and P. guttatus venom. Two 
                lethal myotoxins , both PLA2 basic proteins, II = 127 AA, 
                MW 14170D, LD50 4.5 mg/kg sc mice; IV = 129 AA , MW 14100D, 
                LD50 4.3 mg/kg sc mice. For all toxins described in this 
                study (including Ib and VIIIa above) death occurred in 
                hours due to respiratory paralysis at high doses, but in 
                days due to myolysis and renal failure at lower doses. 
                (Mebs & Samejima 1980) 
                P. coll.
                From P. colletti venom: Lethal PLB protein, dimer, MW 
                33000D in two chains of 16500D, LD50 approx. 2 mg/g ip 
                mice. Causes death due to myolysis and also associated 
                ataxia, respiratory difficulty, possibly neurotoxic, and 
                also strongly haemolytic. (Bernheimer et al 1987) 
                Pa 10a
                From P. australis venom: Lethal single chain PLA2 protein, 
                LD50 0.1 mg/g iv mice. Produces paralysis by reducing 
                acetylcholine release from the terminal axon at the 
                neuromuscular junction, and by direct blockade of muscle 
                fibre contractility. (Rowan et al 1989) 
                Pa 11
                From P. australis venom: Lethal single chain PLA2 protein, 
                LD50 0.23 mg/g iv mice, MW 14000D, 118 AA. Action similar 
                to Pa10a. (Nishida et al 1985, Rowan et al 1989) 
                From P. australis venom: Single chain PLA2 protein, MW 
                13500, 118 AA, initially described as non-lethal, later as 
                lethal at higher doses with an LD50 6.8 mg/g iv mice. 
                Action similar to PA10a. (Nishida et al 1985, Rowan et al 
                Pa a

                From P. australis venom: Single chain protein, 62 AA, MW 
                7100D, LD50 76 mg/kg iv mice. Described as a short chain 
                neurotoxin with considerable homology to similar sea snake 
                neurotoxins, presumably post-synaptic in action. (Takasaki 
                & Tamiya 1985) 
                Pa 1D
                From P. australis venom: Single chain protein, 68 AA, non-
                lethal to mice, considered a long chain neurotoxin 
                homologue. (Takasaki 1989) 
                None isolated. Pseudechis venoms appear to be anticoagulant 
                in vitro rather than procoagulant. (Sutherland et al 1981, 
                Marshall & Herrmann 1983, Campbell 1967, Campbell & 
                Chesterman 1972, Trethewie 1971). They are not noted to 
                have significant platelet activity. (Marshall & Herrmann 
                In vitro haemolytic activity of Pseudechis venoms has long 
                been recognized but few haemolysins have been characterized 
                specifically. Significant activity has been noted for P. 
                australis, P. porphyriacus, P. papuanus, P. colletti. 
                Phospholipase B has been characterized as a haemolytic 
                fraction of P. colletti venom. (Doery & Pearson 1961, 
                Bernheimer et al 1986,1987) 

     3.4  Other chemical contents

          There are few data on most of these components, which include L-
          amino acid oxidase.
          (Trethewie 1971, Takasaki & Tamiya 1982)



     4.1  Uses

          Venom is used both in antivenom production and for laboratory 

     4.2  High risk circumstances

          Children:  when playing in areas where black snakes are common, 
          either through accidental encounter (ie stepping on snake) or 
          while trying to emulate noted naturalists (ie trying to catch 

          Adults:  when living in areas where black snakes are common, and 
          moving around barefoot and without due care, or while putting 
          hands etc into non-reconnoitred potential snake retreats (ie 
          hollow logs etc). 
          Farm workers:  when working in areas where black snakes are 
          Reptile keepers & snake handlers:  if due care is not exercised 
          in catching and handling snakes, including venom milking. 
          Recreation seekers:  camping or walking or playing sport (ie 
          water sports, water skiing) in areas where black snakes are 
          Homes:  around homes in black snake prone areas where water is 
          seasonally scarce and free water is available in the garden or 

     4.3  High risk geographical areas

          No specific high risk areas for black snake bites have been 
          documented. P. porphyriacus most likely to be encountered in 
          wetlands areas and along creeks. P. australis most common in arid 
          central and north Australia where it may be a major cause of 
          snakebite. P. papuanus is common in parts of Papua New Guinea. 


     5.1  Oral

          Not applicable.

     5.2  Inhalation


     5.3  Dermal

          Venom cannot be absorbed through intact skin.

     5.4  Eye

          Not applicable.

     5.5  Parenteral

          5.5.1 Bites

          In human envenomation, venom is always inoculated by the snake 
          biting.  Owing to the size of the fangs, venom is most likely to 
          be inoculated cutaneously or subcutaneously. 

          5.5.2 Stings

          Not possible.

     5.6  Others

          Experimentally venom may be administered to test animals via
          subcutaneous, intramuscular, intravenous, intraperitoneal, and
          intraventricular (CNS) routes.

    6.   KINETICS

     6.1  Absorption by route of exposure

          The rate and amount of absorption will depend on the quantity of 
          venom injected, the depth of injection, site of injection 
          including vascularity, the activity of the victim, and the type, 
          efficiency of application and length of application of first aid. 
          Clinical evidence from human cases of envenomation suggests that 
          much initial venom movement is via the lymphatic pathways. 
          Direct intravenous injection, unrecorded in man, obviously allows 
          rapid systemic circulation of venom and may result in different 
          effects from normal routes of inoculation, particularly in regard 
          to coagulation. 
     6.2  Distribution by route of exposure

          It appears that much venom is transported from the bite site via 
          the lymphatic system, ultimately reaching the systemic 
          circulation.  Experience with human cases of black snake 
          envenomation shows that symptoms and signs of envenomation may 
          occur within 60 minutes of the bite, especially in children, 
          particularly for P. australis bites.  Such early effects (eg 
          headache, nausea, abdominal pain, collapse) may be due to either 
          rapidly systemically circulating venom toxins, or systemically 
          circulating autocoids released at the bite site by the action of 
          venom on local tissue.
          Once in the systemic circulation, venom rapidly reaches high 
          concentrations in the kidneys, whence it is excreted in the 
          urine.  Venom must also exit the circulation and enter the 
          extravascular space, where it binds within target organs.
          The kinetics of venom distribution, excretion, and detoxification 
          are incompletely understood. Coagulopathy potentially may become 
          well established within 30 minutes of a bite, although this is 
          poorly documented for most Pseudechis spp. (P. papuanus is an 
          exception which may cause significant coagulopathy, but there is 
          doubt over the validity of the clinical data on which this is 
          based (Campbell 1967, Campbell & Chesterman 1972). 

     6.3  Biological half-life by route of exposure

          No data

     6.4  Metabolism

          Little information is  available on the metabolism of  venom 
          components in man, but most components are fully active in whole 
          venom and require no  further  modification  for activity.  Venom 
          reaches  high concentrations in the kidneys, where it is excreted 
          in urine.  (Sutherland & Coulter, 1977 a,b). The fate of specific 
          venom components, particularly neurotoxins and procoagulants, is  
     6.5  Elimination by route of exposure

          Most venom appears to be eliminated via the kidneys in the urine.


     7.1  Mode of action

          Neurotoxic paralysis
          Whole venom of at least some species of Pseudechis contains a  
          variable mixture of presynaptic and postsynaptic neurotoxins.  
          Composition of this mixture may not be uniform  across  all  
          populations  of black snakes. However current clinical case data 
          and some animal experimental work indicates that neurotoxic 
          envenomation by these snakes is either not seen or is of minor 
          extent. It should be noted that relatively few case reports are 
          available for most species thus the issue of paralysis due to 
          Pseudechis bites remains unresolved. 
          Procoagulants and coagulopathy
          No procoagulants have been isolated from Pseudechis venoms, which 
          distinguishes these venoms from those of other major Australian 
          snakes (Notechis, Oxyuranus, Pseudonaja, Tropidechis) which 
          contain potent procoagulants. Early research suggested that 
          Pseudechis venoms have a procoagulant action in vitro but it now 
          appears that its action is anticoagulant. 
          Early clinical work in Papua New Guinea suggested P. papuanus 
          caused a defibrination-type coagulopathy in man (Campbell 1967), 
          but subsequent reviews have indicated that this was probably 
          false due to misidentification of the snake. Experimental 
          evidence clearly supports the anticoagulant action of these 
          venoms (Campbell & Chesterman 1972, Marshall & Herrmann 1983). 
          P. papuanus has a potent anticoagulant action in vitro with 
          inhibition of thromboplastin generation, and inhibition of 
          conversion of prothrombin to thrombin (Campbell & Chesterman 
          1972). Anticoagulant action and lack of procoagulant action was 
          shown with in vitro experiments using P. papuanus and P. 
          australis venom (Marshall & Herrmann 1983). This latter work 
          showed a slight coagulant effect without apparent anticoagulant 

          effect for P. porphyriacus venom. In vivo experiments using 
          monkeys demonstrated an apparent "coagulopathy" using P. 
          australis venom, with prolongation of partial thromboplastin time 
          and prothrombin time, but no comment on fibrinogen levels and FDP 
          were made, thus these results are equally consistent with an 
          anticoagulant action (Sutherland et al 1981). 
          While some presynaptic  neurotoxins  are  also   directly 
          myolytic (eg notexin) and cause major destruction of skeletal 
          muscle, locally and systemically (Harris et al 1975), both in 
          experimental animals and occasionally in human envenomation, some 
          Pseudechis venoms contain direct myotoxins which do not appear to 
          exert significant neurotoxic activity. However these myotoxins, 
          which have been found in all Pseudechis venoms searched (eg. P. 
          australis, P. porphyriacus, P. colletti, P. guttatus), do appear 
          to be mostly PLA2 toxins closely related to the myotoxic 
          presynaptic neurotoxins. Based on extensive work with these 
          latter toxins the mode of action of Pseudechis myotoxins may be 
          inferred. The phospholipase  A2  activity  of  these toxins may 
          hydrolyse muscle cell membrane phospholipids (Mebs & Samejima 
          1980).  Not all muscle cells are equally  affected,  skeletal  
          muscle  being  most susceptible,  and immature muscle cells 
          appear resistant.  In experimental animals muscle cell 
          destruction may occur in only a  few hours; within 3 days  the 
          process is complete and cell regeneration commences, with 
          complete regeneration taking 3-4 weeks (Harris et al 1975).  
          Following acute muscle  damage there is a progressive rise  in 
          serum  levels of  creatine kinase (CK) peaking  at 10 - 20 hours  
          post-bite.  Myoglobin levels  also rise  and are excreted in  the 
          urine, causing the typical dark brown discolouration (Sutherland 
          et al 1981b). 
          In humans, the  peak CK may be extraordinarily high (up to 
          300,000 U/l or more), and myoglobinuria may  continue for many 
          days (for example, the maximum is 11 days for N. ater niger bite) 
          (White, unpublished data; Hood and Johnson, 1975). Data on human 
          cases of Pseudechis envenomation with myolysis is scant, but the 
          author's experience is that P. australis bites often cause severe 
          myolysis but  bites by P. porphyriacus and P. guttatus do not. 
          Renal damage
          No specific  nephrotoxins have  been detected in Pseudechis snake 
          venom, and no clear cases of renal function impairment have been 
          reported in humans envenomed by Pseudechis. However, a fatal case 
          of P. australis envenomation did show evidence of renal damage at 
          autopsy, possibly secondary to extensive myolysis (Rowlands et al 

     7.2  Toxicity

          7.2.1 Human data


                     The  human lethal dose for Pseudechis venoms is 
                     unknown. However,  without antivenom treatment, a 
                     significant number of  P. australis bites will prove 
                     fatal. The same may apply for P. papuanus and possibly 
                     P. butleri (for which there are no human case 
                     reports), but for P. porphyriacus, and possibly P. 
                     colletti and P. guttatus human fatalities are very 
                     rare, and envenomation by these species is very 
                     unlikely to be life threatening, except perhaps in a 
                     small child. 


                     No data available, but clearly the smaller body mass 
                     of  a child compared to available venom ensures that 
                     children are more likely  to receive  a lethal dose 
                     than adults. 

          7.2.2 Relevant animal data

                Snake                  LD50 mg/kg sc mice
                P. australis              2.38
                P. butleri                no data
                P. colletti               2.38
                P. guttatus               2.13
                P. papuanus               1.09
                P. porphyriacus           2.52

          7.2.3 Relevant in vitro data

                No data available.

     7.3  Carcinogenicity

          No data available. 

     7.4  Teratogenicity

          No data available. 

     7.5  Mutagenicity

          No data available. 

     7.6  Interactions

          No data of clinical significance.


     8.1  Material sampling plan

          8.1.1 Sampling and specimen collection

         Toxicological analyses

                     For venom detection: swab from bite site moistened in 
                     sterile saline.  If there is systemic envenomation, 
                     also collect urine (5ml in sterile container).
                     For venom analysis (research only using 
                     radioimmunoassay): 5ml blood; 5ml urine, frozen.
                     At autopsy collect vitreous humor, lymph nodes 
                     draining bite area, excised bite site.
                     (For other laboratory tests see 10.2.1)

         Biomedical analyses

                     For standard tests (eg. serum/plasma electrolytes, CK, 
                     creatinine, urea) collect venous blood in a container 
                     with appropriate anticoagulant as issued by the 
                     laboratory (usually heparin). 

         Arterial blood gas analysis

                     Collect arterial blood by sterile arterial puncture 
                     into a container as issued by the laboratory. 

         Haematological analyses

                     For whole blood clotting time as a "bedside" test 
                     collect 5-10 ml of venous blood without anticoagulant 
                     (either in the collection syringe or from a central 
                     line or other venous access line that may have 
                     anticoagulant) and place in a glass test tube. 
                     Carefully observe the time till a clot appears.

                     For standard tests (eg. coagulation studies, complete 
                     blood picture) collect venous blood in appropriate 
                     containers with anticoagulant as issued by the 
                     laboratory ensuring that the right amount of blood is 
                     used (for coagulation studies citrate will usually be 
                     the anticoagulant, and EDTA will be used for complete 
                     blood pictures). 

          8.1.2 Storage of laboratory samples and specimens

       Toxicological analyses

                For samples for standard venom detection:
                Short term (less than 24 hrs) ordinary fridge is acceptable 
                -(4C), in sterile container. 

                Long term, store frozen (-20C or lower).
                For samples for venom analysis (research) store frozen (-
                200C or lower). 
                For samples for standard tests refer to laboratory. In 
                general keep at 4C, particularly for samples for 
                coagulation studies.

          8.1.3 Transport of laboratory samples and specimens

       Toxicological analyses

                Use insulated container.

     8.2  Toxicological analyses and their interpretation

          8.2.1 Tests on toxic ingredient(s) of materials

         Simple qualitative test(s)

                     A simple qualitative test for presence of snake venom 
                     and designation of species/genus  group, corresponding 
                     to the most appropriate monovalent anti-venom is a 
                     commercial test sold by antivenom manufacturer as a 
                     kit (Snake Venom Detection Kit; CSL Melbourne) 
                     (Coulter et al 1980; Chandler & Hurrell 1982; Hurrell 
                     & Chandler 1982). 
                     (1)  Principle of test
                     The kit uses an enzyme-linked immunosorbent assay 
                     technique with specific antibodies raised to each of 
                     the five main venom types in Australia.  If venom is 
                     present in the test sample it will cause a colour 
                     change in the relevant well of the kit, indicating the 
                     presence of venom for that species. 
                     (2)  Sampling
                     See section 8.1.  The best samples are a swab from the 
                     bite site (swab stick etc. included in kit), or urine 
                     (only if patient has systemic envenomation).  Blood 
                     has not proved a reliable sample (White 1987d). 
                     (3)  Chemicals and Reagents
                     All reagents needed for the test are included in the 
                     kit.  The kit should be kept at 4C (standard fridge) 
                     and has a shelf life of 6 months.  A control is built 
                     into the kit.  If this fails the test results are 
                     (4)  Equipment
                     Virtually all equipment required for the test is 

                     provided in the kit.  The only item not provided is a 
                     timer, but an ordinary watch is sufficient, each step 
                     taking approximately 10 minutes.  An empty specimen 
                     container in which to discard waste fluid at each step 
                     is a useful addition. 
                     (5)  Specimen preparation
                     Not applicable
                     (6)  Procedure
                     Refer to instructions in kit
                     (7)  Calibration procedure
                     Not applicable
                     (8)  Quality control
                     Included in kit
                     (9)  Specificity
                     Where testing for snake venom using a bite site swab 
                     or urine, no interference with a result is expected.  
                     If snake venom is present it will react with specific 
                     antibody in one of the wells, resulting finally in a 
                     colour change in that well. After a further delay all 
                     wells will then change colour.  It is therefore 
                     important to carefully watch the wells in the last 
                     stage and note which tube changes colour first.  A few 
                     snakes may cause simultaneous colour change in two 
                     wells initially. This is particularly true for P. 
                     porphyriacus, P. colletti and P. guttatus which may 
                     cause simultaneous colour change in wells for both 
                     mulga snake venom and tiger snake venom. 
                     (10) Detection limit
                     The manufacturer states the kit will detect 
                     concentrations of venom as low as 10 ng/ml. 
                     (11) Analytical assessment
                     Not applicable
                     (12) Medical interpretation
                     If the test is positive, it will indicate the presence 
                     of snake venom and the species/genus of snake and 
                     therefore the appropriate monovalent antivenom to 
                     neutralize the effects of that venom. Note however 
                     that for some species of Pseudechis there may be a 
                     colour change in two tubes simultaneously which may 
                     cause confusion. This most often is manifest by change 

                     in the tubes for both mulga snake and tiger snake 
                     If the test sample was a bite site swab, a positive 
                     result does not indicate either the presence of 
                     systemic envenomation, or the need to administer 
                     antivenom.  Other clinical criteria are required in 
                     this situation (see sections 9 and 10). 
                     If the test sample was urine a positive result 
                     indicates present or past systemic envenomation and 
                     together with other clinical and laboratory criteria 
                     may be used to determine the need for antivenom 

         Advanced qualitative confirmation test(s)

                          as for

         Simple quantitative method(s)

                     Not applicable

         Advanced quantitative method(s)

                     A  radioimmunoassay  has been developed  by   staff  
                     at  the Commonwealth  Serum Laboratories,  Melbourne 
                     to detect small quantities of many Australian snake 
                     venoms.  It is  primarily a  research tool, being too 
                     time consuming to be practical in determining 
                     emergency treatment of snakebite victims.  It has 
                     proved  useful in demonstrating snake venom either at 
                     autopsy or after patient recovery. 

          8.2.2 Tests for biologicals specimens

         Simple qualitative test(s)


         Advanced qualitative confirmation test(s)


         Simple quantitative method(s)

                     Not applicable

         Advanced quantitative methods(s)


         Other dedicated methods(s)

                     No data available.

          8.2.3 Interpretation of toxicological analyses

                For venom detection as for subsection (12):
                If the test is positive, it will indicate the presence of 
                snake venom and the species/genus of snake and therefore 
                the appropriate monovalent antivenom to neutralize the 
                effects of that venom. 
                If the test sample was a bite site swab, a positive result 
                does not indicate either the presence of systemic 
                envenomation, or the need to administer antivenom.  Other 
                clinical criteria are required in this situation (see 
                sections 9 and 10). 

                If the test sample was urine a positive result indicates 
                present or past systemic envenomation and together with 
                other clinical and laboratory criteria may be used to 
                determine the need for antivenom therapy. 

                For venom analysis refer to the laboratory performing the 

     8.3  Biomedical Investigations and Their Interpretation:
          8.3.1 Biochemical analyses

         Blood, plasma or serum

                     Electrolytes: Look for imbalance, particularly 
                     evidence of dehydration, hyponatraemia (inappropriate 
                     ADH syndrome?), hyperkalaemia (renal damage, 
                     Urea, creatinine: Look for evidence of renal function
                     CK: If high may indicate rhabdomyolysis, usually 
                     greater than 1000 U/l. 


                     Output: Low output may be due to renal damage or poor 
                     fluid input. 
                     Myoglobin: If present indicates rhabdomyolysis, and 
                     may be missed as the red colouration of urine may be 
                     mistaken for haematuria (both may be positive on dip 
                     stick testing). 
                     Electrolytes: if indicated (eg. inappropriate ADH 

         Other biological specimens

                     No data

          8.3.2 Arterial blood gas analysis

                Performed in the setting of impaired respiratory function, 
                usually secondary to neurotoxic paralysis; look for 
                evidence of poor oxygenation and its sequelae. 

          8.3.3 Haematological analyses

                Whole blood clotting time: If greater than 10 mins suspect 
                presence of coagulopathy and if no clot after 15 mins then 
                significant coagulopathy present. If no clot after 30 mins 
                then full defibrination is likely. 
                Coagulation studies: If possible these should be performed 
                as well as or instead of whole blood clotting time as they 
                will give a more comprehensive picture of any coagulopathy. 
                The principal defect is likely to be a defibrination-type 
                coagulopathy, which will render the blood unclottable. 
                This will usually result in the following key results:
                Prothrombin ratio /INR   >12 (normal about 0.8-1.2).
                APTT                     >150 secs (normal <38 secs).
                Thrombin clotting 
                 time (TCT)              > 150 secs (normal <16 secs).
                Fibrinogen               <0.1 g/l (normal 1.5-4.0 g/l).
                Fibrin(ogen) degradation 
                products                 grossly elevated 
                                         (including D-Dimer).
                Platelet count            normal.
                If the patient exhibits the above picture in the context of 
                a snakebite then they have a defibrination-type 
                coagulopathy. This will require specific antivenom therapy 
                (see section 10) and repeated tests of coagulation status 
                to define progress of the coagulopathy and titrate 
                antivenom therapy against resolution. The earliest sign of 
                resolution will be a rise in fibrinogen level and this may 
                first be seen as a reduction in the TCT from > 150 secs, 
                often to 80 secs or less. This may occur before there is a 
                detectable rise in fibrinogen titre. It indicates that the 
                pathologic process of venom-induced defibrination has 
                ceased. This implies that all circulating venom has been 
                neutralized, at which point further antivenom therapy can 
                be withheld until the trend of improving results is 
                confirmed. No further antivenom therapy for the 
                coagulopathy is indicated (unless there is a subsequent 
                In the patient seen late or initially treated elsewhere 
                there may be no abnormal clotting time (INR < 2.0) but 
                fibrinogen may be low and associated with raised 
                degradation products. In this case the results may indicate 
                a minor or resolved coagulopathy not requiring antivenom 

                therapy. Note that the platelet count (complete blood 
                picture) will usually be normal despite the intense 
                In a few cases the platelet count may start to fall as or 
                after resolution of the defibrination occurs. This is 
                usually associated with renal damage and renal function 
                should be assessed. In this setting the thrombocytopenia 
                may well be secondary to the renal damage.

          8.3.4 Other (unspecified) analyses

          8.3.5 Interpretation of biomedical investigations

                The interpretation of the above tests should be made in the 
                context of total patient assessment including clinical 
                evidence of pathology such as paralysis, myolysis, 
                coagulopathy and renal damage. 

     8.4  Other Biomedical Investigations and Their Interpretation

          While other investigations are not usually required to make the 
          primary diagnosis of snakebite envenomation, they may be 
          indicated in response to secondary effects of envenomation. If 
          there is either renal failure or severe rhabdomyolysis there may 
          be a hyperkalaemia, hence an ECG may be appropriate. If the 
          patient is unconscious, especially in the presence of a severe 
          coagulopathy, then a CT head scan may be appropriate to determine 
          if there is intracranial pathology such as a haemorrhage. 

     8.5  Summary of most essential biomedical and toxicological analyses 
          in acute poisoning and their interpretation 

          Overall interpretation of the results of the above tests will 
          depend on the clinical setting. These results should never be 
          interpreted in isolation from an overall clinical assessment. 
          A patient with positive venom detection from either the bite site 
          or urine and a significant coagulopathy clearly is envenomed and 
          will usually require antivenom therapy. 
          A patient with positive venom detection from the bite site only 
          and with no clinical symptoms or signs of envenoming and all 
          other tests negative is not significantly envenomed at that point 
          in time and does not require antivenom therapy. However this 
          situation may change and so careful observation and repeat 
          testing would be indicated. 
          A patient presenting some hours after the bite with positive 
          venom detection from the urine but clinically well and with all 
          other tests either normal or showing a resolved coagulopathy, 
          probably had a minor degree of envenomation which is now resolved 
          and will usually not require antivenom therapy. However they 
          should be observed carefully for evidence of relapse. 


     9.1  Acute poisoning/envenomation

          9.1.1 Ingestion

                No data available.

          9.1.2 Inhalation

                No data available.

          9.1.3 Skin exposure

                If skin surface intact, no effects.

          9.1.4 Eye contact

                No data available.

          9.1.5 Parenteral exposure

                In practical terms, subcutaneous or intradermal injection 
                is the only likely route of entry. 
                Early symptoms (usually in the first six hours).
                Local:  pain, mild to  severe; oedema,  mild; ecchymosis, 
                variable, mild;  pain or swelling of draining  lymph nodes 
                (may take 1-4 hours to develop). 
                Systemic:  collapse, unconsciousness, convulsions may all 
                occur, especially in children, occasionally  as  rapidly  
                as  15  minutes after the bite.  Headache, nausea, 
                vomiting, abdominal pain, and visual disturbance may all 
                Delayed symptoms
                Local:  rarely a small area of superficial necrosis may 
                develop, particularly if first aid is left in place more 
                than 4 hours, or if a tourniquet is used (Sutherland 1981, 
                1983a; White 1987d; Frost, 1981). 
                Myolysis - muscle weakness and movement pain.   Dark urine. 
                Renal impairment - oliguria or anuria. Paralysis and 
                coagulopathy not convincingly reported.

          9.1.6 Other

                No data

     9.2  Chronic poisoning by: 

          9.2.1 Ingestion

                No data available.

          9.2.2 Inhalation

                No data available.

          9.2.3 Skin exposure

               No data available.

          9.2.4 Eye contact

                No data available.

          9.2.5 Parenteral exposure

                No data available.

          9.2.6 Other

                No data available.

     9.3  Course, prognosis, cause of death

          Initially the patient will usually be anxious, knowing they have 
          sustained a snakebite.  The subsequent course will depend on (a) 
          amount of venom injected, (b) size of patient relative to venom 
          load (ie children may be worse affected), (c) degree of activity 
          of patient after bite (physical activity hastens venom 
          absorption), (d) timing, type, effectiveness of first aid, (e) 
          speed and nature of specific medical treatment given, if systemic 
          envenomation ensues, (f) pre-existing health factors for each 
          patient (ie past renal problems, allergic problems etc). 
          Bites will vary in severity with the species of black snake 
          involved in addition to the factors mentioned above. 
          P. australis:    Potentially moderate to severe bite, 
                           potentially lethal.
          P. butleri:      As above (no human case data).
          P. papuanus:     As above.
          P. porphyriacus: Generally mild bites, not lethal in adults 
                           in general.
          P. colletti:     As for P. porphyriacus (little human case data)
          P. guttatus:     As for P. porphyriacus (little human case data).
          Minor envenoming:  little or no venom injection, no development 
          of systemic envenomation, no need for antivenom treatment, no 
          likely sequelae or complications. 
          Moderate envenoming:  bite usually at least slightly painful, 
          with some local reactions usually including local swelling and 
          sometimes ecchymosis, subsequent development over the next few 

          hours of some or all of the following:  headache, nausea, 
          vomiting, abdominal pain, collapse, and possibly convulsions 
          (more likely in children). 
          On the evidence of current human case data, paralysis is unlikely 
          to occur following Pseudechis envenomation but caution dictates 
          that it should at least be sought; early signs include ptosis and 
          diplopia. The same applies to coagulopathy which, if present, is 
          most likely due to true anticoagulation rather than 
          defibrination; however, laboratory evidence of coagulopathy 
          should be sought.  
          Antivenom treatment at this stage may arrest or reverse the 
          various manifestations of systemic envenomation.  Without 
          antivenom treatment, in most  cases of P. australis, P. papuanus, 
          and probably P. butleri envenomation, the symptoms and signs will 
          show progressive worsening. Progressive myolysis and muscle 
          movement pain; and secondary renal failure are particular risks; 
          secondary complications of the above, particularly pneumonia, 
          should be considered. The ultimate outcome may be death, more 
          than 24 hours post-bite. 
          For bites by P. porphyriacus, and probably P. colletti and P. 
          guttatus, the clinical picture is in general less severe. There 
          may be quite significant local symptoms (especially swelling and 
          pain) and some systemic symptoms (headache, nausea, vomiting, and 
          abdominal pain). It is rare for other problems to occur. 
          Specifically it appears that significant myolysis and renal 
          damage are not seen, and most bites with envenomation are not 
          life-threatening and, at least in healthy adults, may not require 
          antivenom therapy. 
          Severe envenoming:  most likely if the bite is either multiple, 
          or associated with a chewing bite and numerous teeth marks. P. 
          porphyriacus, P. colletti, P. guttatus bites are not likely to be 
          lethal. Severe envenoming is only likely after bites by P. 
          australis, P. butleri, P. papuanus. Note that, as with any form 
          of envenomation, atypical cases may occur which are more severe 
          than might be expected for that species. 
          The following applies to bites by P. australis, P. butleri, P. 
          papuanus. Local reactions such as ecchymosis, oedema and pain 
          likely.  Rapid development of headache, and possibly collapse, 
          and convulsions (especially children), sometimes within 30 
          minutes of bite.  Subsequent symptoms may include headache, 
          nausea, vomiting, abdominal pain, and evidence of progressive  
          myolysis and renal impairment. Paralysis and defibrination-type 
          coagulopathy are not likely on the evidence of current case data 
          (although research data suggest that paralysis may be possible). 
          However, myolysis may mimic some features of paralysis due to 
          muscle movement pain and intrinsic weakness. Features of 
          paralysis should be looked for such as ptosis and diplopia. 
          Myolysis may take several hours to develop.  Renal damage may 
          occur early.  Prompt antivenom treatment is required as soon as 
          nature of envenomation evident.  The myolysis may not be 
          preventable, and may result in widespread muscle damage, which 

          will eventually resolve.  Renal damage is probably reversible, 
          after a period of dialysis. 
          Without antivenom treatment  patients with severe envenoming may 
          Special notes
                Children are more likely to develop severe envenomation 
                than adults, and do so more rapidly. 
                Bites to the trunk or face may cause earlier development of
                Secondary infection of the local bite wound may occur.
                Physical activity after a snakebite increases the rate of 
                absorption of venom and so hastens the onset of 
                envenomation.  This situation often occurs in bites to 
                Multiple bites nearly always are associated with more 
                severe envenomation. 
                In the past, perhaps as many as 30% of all P. australis 
                snake bites have proved fatal when no antivenom treatment 
                was used. No data are available on the fatality rate 
                associated with antivenom treatment, but deaths do still 
                occur.The situation with P. papuanus and P. butleri is 
                probably similar or less severe. For P. porphyriacus it is 
                clear that very few deaths have occurred, and probably none 
                in normal healthy adults, but children and the elderly may 
                be at more risk. This should be born in mind when deciding 
                on the merits of antivenom therapy as the subjective 
                symptomatology for the patient may be worse than the degree 
                of envenomation actually present. Bites by P. colletti and 
                P. guttatus are probably similar in severity to those of P. 
                porphyriacus, although case data are lacking, and there are 
                no known fatalities. 
          Causes of death
                Myolysis            This appears to be the major clinical
                                    problem. Fatal cases poorly
                Renal Failure       Includes secondary complications such
                                    as infections.
                Anaphylaxis         Acute allergic reaction to venom in a
                                    patient previously exposed to
                                    Pseudechis  snake venom (eg reptile

                Cardiac complications likely to be secondary, and their 
                                    role in Pseudechis snake bite 
                                    fatalities uncertain.

     9.4  Systematic description of clinical effects

          9.4.1 Cardiovascular

                Collapse, presumably due to hypotension, is seen in the 
                early stages of systemic envenomation at least by P. 
                australis, especially in children. The mechanism is 
                uncertain but may be due to release of vasoactive 
                Specific cardiac abnormalities due to Pseudechis 
                envenomation in man are not described. 

          9.4.2 Respiratory

                No primary effects of Pseudechis venom on the respiratory 
                system in man are reported. 

          9.4.3 Neurological


                     No direct CNS toxins have been reported for Pseudechis 
                     venom, early collapse and convulsions may occur, 
                     especially in children.  Their aetiology remains 

         Peripheral nervous system

                     Effect of venom uncertain and of little clinical 


                     Abdominal pain.

         Skeletal and smooth muscle

                     Pseudechis venom has been shown to act at the 
                     neuromuscular junction experimentally but not 
                     clinically. Presynaptic  neurotoxins are present but 
                     their clinical significance is uncertain. 
                     Theoretically, they may cause progressive 
                     neuromuscular paralysis, up to complete paralysis of 
                     all muscles of respiration. No documented cases. 

          9.4.4 Gastrointestinal

                Nausea and vomiting may occur.  In the presence of a venom-
                induced coagulopathy, haematemesis and even melaena may 
                occur, though they appear rare, even in severe 
                envenomation.  Abdominal pain is sometimes described. 

          9.4.5 Hepatic

                Direct hepatic effects of Pseudechis venom have not been 
                noted clinically or experimentally. 

          9.4.6 Urinary


                     No direct nephrotoxin has been reported from 
                     Pseudechis venom, nor has renal failure  been reported 
                     but in one fatal case there was evidence of renal 
                     damage, and it is potentially a very serious 
                     complication of envenomation.  The nature of the renal 
                     injury and its cause are poorly documented, but acute 
                     tubular necrosis seems most likely. 

                     No data available.

          9.4.7 Endocrine and reproductive systems

                No data available.

          9.4.8 Dermatological

                The local bite site is often painful, with significant 
                swelling, and ecchymosis is sometimes seen.  Teeth marks 
                are variable, from single fang puncture to multiple tooth 
                punctures and scratches. Local necrosis may occur, but is 
                usually minor if present, unless a tourniquet is used as 
                first aid.  Secondary infection may occur (White 1983b). 

          9.4.9 Eye, ear, nose, throat: local effects

                No data available.

          9.4.10 Haematological

                A major clinical effect of most Australian  snake 
                envenomation in man is coagulopathy caused by potent 
                procoagulants in the venom, which cause prothrombin 
                activation and secondary fibrinogen consumption. Initially, 
                this was also thought to be true of Pseudechis bites, 
                especially P. papuanus and P. australis. It now appears 
                this is not so and therefore major bleeding is not likely. 
                However, minor bleeding problems associated with the 
                anticoagulant effect of the venom may occur.
                An early neutrophil leukocytosis may occur in some patients.
                Significant depletion of circulating lymphocytes may occur 
                in the early stages of envenomation, with resultant 

          9.4.11 Immunological

                No data available.

          9.4.12 Metabolic

        Acid base disturbances

                     No changes.

        Fluid and electrolyte disturbances

                     Secondary fluid and electrolyte disturbances due to 
                     renal failure (if present), or myolysis may occur. 
                     Beware particularly of hyperkalaemia.
                     The possibility of inappropriate ADH (antidiuretic 
                     hormone secretion) syndrome should be considered.  In 
                     this situation, otherwise acceptable intravenous fluid 
                     loads may result in significant electrolyte imbalance 
                     and other sequelae. 


                     Rise in serum levels of liver enzymes and CK (if 
                     rhabdomyolysis occurs).  A rise in CK to below 1000 
                     U/l is not indicative of rhabdomyolysis.  True venom-
                     induced rhabdomyolysis causes CK levels well above 
                     1000 U/l. 

          9.4.13 Allergic reactions

                May occur due to allergy to venom or antivenom, and 
                resultant anaphylaxis may prove fatal.
                Reptile keepers previously bitten by black snakes are also 
                at risk of acute anaphylactic allergic reactions on 
                subsequent bites, which may cause collapse within minutes 
                of the bite.  Fatalities have occurred due to this 
                mechanism with other species (Notechis), and the author is 
                aware of severe non-fatal acute allergic type reactions 
                following bites by P. porphyriacus (Sutherland 1983; White 
                1987 b,d, White unpublished observations). 

          9.4.14 Other clinical effects


                Due to direct action of myotoxins on muscle cells, causing 
                widespread muscle damage. This causes muscle weakness, 
                muscle tenderness, muscle movement pain, diminished deep 
                tendon reflexes, rise in serum CK, and myoglobinuria (dark 
                brown urine). If muscle damage is severe, recovery may take 

                weeks, although full functional recovery is possible.  
                Severe muscle wasting may be apparent, and intensive 
                physiotherapy is required to prevent contractures in the 
                early stages, and to promote rapid muscle regeneration in 
                the later stages. 

          9.4.15 Special risks

                No data available. 

     9.5  Others

          No data available.


     10.1 General Principles

          All patients suspected of having sustained a Pseudechis bite 
          should be admitted to hospital for observation over the first 24 
          hours.  While all such cases should be treated as potentially 
          fatal, not all will develop envenomation.  Management of cases 
          with systemic envenomation may be divided into specific, 
          symptomatic, and general treatment. 
          The aims of treatment are:
          (a)   Maintain life by supporting vital bodily functions.
          (b)   Neutralise inoculated venom.
          (c)   Correct venom-induced abnormalities.
          (d)   Prevent or correct secondary complications.
          Specific treatment
          If there is evidence of systemic envenomation, antivenom therapy 
          is the most important treatment.  Once the snake has been 
          identified (eg by venom detection) consider  giving specific 
          antivenom depending on the clinical situation and the species of 
          snake involved (see section 9). Bites by P. australis, P. 
          papuanus, and probably P. butleri will require antivenom therapy 
          (CSL Black Snake Antivenom). 
          Bites by P. porphyriacus, and probably P. colletti and P. 
          guttatus often may not require antivenom therapy despite systemic 
          envenomation (especially in adults, see section 9), and if 
          antivenom is required then CSL Tiger Snake Antivenom is preferred 
          (cheaper and of lower volume) (White 1981; 1987d; Sutherland 
          1983; Trinca 1963). 
          Symptomatic and general treatment
                Support of cardiorespiratory systems.
                Treatment of shock.
                Maintain adequate renal perfusion.
                Tetanus prophylaxis.
                Avoid respiratory depressant medications (eg morphine).

                Avoid antiplatelet medications (eg aspirin).

     10.2 Relevant laboratory analysis and other investigations

          10.2.1 Sample collection

                Venom for venom detection:  use CSL Venom Detection Kit; 
                best sample is swab from bite site (swab stick etc in kit); 
                if systemic envenomation present then urine is useful but 
                serum or plasma are less reliable.  If bandage applied over 
                bite site as first aid, keep bandage adjacent to wound, as 
                this may also have venom absorbed, and could be tested for 
                venom (after elution) if all other samples negative in 
                presence of significantly envenomed patient. 
                Blood:  Initially collect for complete blood count (EDTA 
                sample), clotting studies (citrated sample), electrolytes 
                and enzymes (heparin and/or clotted sample).  In 
                anticoagulated blood samples ensure correct ratio of blood 
                to anticoagulant (especially citrate samples) and proper 
                mixing.  If laboratory facilities unavailable, collect for 
                whole blood clotting time (ie 5-10 ml in glass test tube, 
                and measure time to clot).  Samples for clotting studies in 
                particular should be kept cold during transportation. 
                Urine:  Measure urine output, visual check for 
                haemoglobinuria or myoglobinuria (dark red-brown urine); if 
                suspect myoglobinuria collect samples at intervals for 
                subsequent laboratory confirmation (5-10 ml). 

          10.2.2 Biomedical analysis

                Venom detection:  Venom at the bite site confirms only the 
                species of snake, but venom in the urine indicates systemic 
                Coagulation studies:  In the absence of a haematology 
                laboratory, whole blood clotting time is a useful test. 
                If a laboratory is available, the most useful tests for 
                presence and extent of coagulopathy are: prothrombin 
                time/ratio; activated partial thromboplastin time; thrombin 
                clotting time; fibrinogen assay; fibrin(ogen) breakdown 
                products assay. 
                In addition, a complete blood count should always be 
                performed concurrently, particularly for a platelet count.
                Other blood tests:
                     Electrolytes (eg Na, K etc);
                     Renal function (eg creatinine, urea);
                     Enzyme levels, especially CK;
                     Arterial blood gas, if appropriate (ie impaired 
                     respiratory function).

                Urine:  For myoglobinuria

          10.2.3 Toxicological analysis

                Venom detection, see section 8.

          10.2.4 Other investigations.

                As indicated medically.

     10.3 Life supportive procedures and symptomatic treatment

          Antivenom therapy, maintenance of adequate renal diuresis and, in 
          the latter stages during recovery, appropriate diet (high 
          protein) and physiotherapy. Carefully monitor for hyperkalaemia, 
          both directly, and by ECG changes. 
          Renal failure
          First priority is to avoid renal injury by ensuring adequate 
          renal perfusion. In all cases of significant systemic 
          envenomation, catheterisation of the bladder to monitor urine 
          output constantly is advisable.  In severe cases of envenomation, 
          the use of a CVP line will assist in adjusting IV fluid load to 
          ensure adequate blood volume and renal perfusion. 
          Once renal injury is established, standard techniques of medical
          management should apply.  Dialysis may be required. 
          Local bite site
          The bite site should be cleaned only after adequate sampling for 
          venom. Local infection may occur, but is not usual, and thus 
          prophylactic antibiotic therapy is not appropriate.  Tetanus 
          prophylaxis should be ensured.  If there is minor local necrosis, 
          this can usually be successfully treated conservatively.  Only 
          rarely will local skin necrosis be sufficient to warrant 
          debridement and grafting, and this is best left until the acute 
          phase of envenomation is over, and the area of injury clearly 
          delineated. Pseudechis  bites do not apparently cause sufficient 
          local reaction to justify surgical decompression, although local 
          swelling can be quite severe, and extend to involve most or even 
          all of the bitten limb, and occasionally the adjacent trunk 
          (especially bites by P. australis).  If compartment syndrome is 
          suspected, then it should be confirmed by intracompartmental 
          pressure measurement prior to any surgical intervention. 
          The principal method of treatment of defibrination-type 
          coagulopathy is the neutralisation of all inoculated venom by 
          antivenom. However, it is unclear whether this applies to the 
          mild anticoagulant type problems seen with some Pseudechis 
          envenomations, most notably due to bites by P. australis and P. 

          In cases of severe envenomation a central venous pressure (CVP) 
          line may be highly desirable for patient management, but in the 
          presence of coagulopathy should be inserted with great caution 
          due to the likelihood of significant haemorrhage from the 
          insertion site if the attempt is unsuccessful. For similar 
          reasons, venepuncture from major veins, such as the femoral, 
          should be avoided, and used only as a last resort. 
          In severe cases of systemic envenomation by Pseudechis species, 
          where antivenom treatment has been delayed, it is possible 
          paralysis may occur and even progress to complete or near 
          complete respiratory paralysis although there are no documented 
          human cases (compare with some cases from Papua New Guinea of P. 
          papuanus envenomation, which may have actually been due to 
          Oxyuranus scutellatus canni, a species known to cause paralysis).  
          In this situation early intervention by endotracheal intubation 
          and artificial ventilation may be lifesaving. Based on experience 
          with other species from Australia, such respiratory support may 
          be needed for hours, days, or even weeks, until adequate 
          respiratory function returns. Once established, severe paralysis 
          might not be reversible by antivenom therapy. 
          Analgesia may be necessary, though most cases will need no more 
          than paracetamol.  Morphine should be avoided (CNS depressant 
          effect). Platelet-active drugs should be avoided (eg aspirin). 
          Steroids may be useful in treatment of severe allergic reactions, 
          or in the prophylaxis of serum sickness, but their role in the 
          general treatment of Pseudechis snake bite is doubtful. 

     10.4 Decontamination

          Not applicable.

     10.5 Elimination

          Not applicable.

     10.6 Antidote/antivenin treatment

          10.6.1 Adults

          Antivenom (CSL, Melbourne) is the specific treatment of 
          Pseudechis snake bite. Two specific antivenoms and Australian 
          polyvalent antivenom are each effective. The type of monovalent 
          (specific) antivenom most appropriate depends on the species of 
          Pseudechis and the two groups will be discussed separately below 
          (Trinca 1963; Sutherland 1974, 1983b; White 1981, 1987d). 

          For bites by P. australis, P. butleri and P. papuanus, the 
          preferred antivenom is CSL Black Snake Antivenom. One ampoule 
          contains 18,000 units of activity against mulga snake (P. 
          australis) venom, but is active against venoms of all other 
          members of the genus. The antivenom is a refined horse serum 
          (Fab2 fragments), with all the potential hazards of that product. 
          This is sufficient to neutralise the "average" amount of venom 
          produced by a single milking of one snake (Pseudechis australis).  
          In a severe bite, and multiple bites, several ampoules of 
          antivenom may be necessary.  The average volume of Black Snake 
          antivenom (horse serum) per ampoule is 35 ml, but the precise 
          volume varies from batch to batch. 
          For bites by P. porphyriacus, P. colletti and P. guttatus, 
          antivenom is not often required, even in the presence of general 
          systemic symptoms, because major envenoming is very rare and the 
          mortality rate is very low (possibly only one recorded case). The 
          quantity of venom produced by these snakes is also less than for 
          the mulga snake and therefore only a third of one ampoule of 
          Black Snake Antivenom is recommended as a standard dose. However 
          CSL Tiger Snake Antivenom is also active against the venoms of 
          these three Pseudechis species, the equivalent dose being one 
          ampoule. As this will be a lower volume of antivenom, it is 
          theoretically safer and less likely to result in side effects. 
          The cost of Tiger Snake Antivenom is also much less than Black 
          Snake Antivenom, and therefore the current recommendations are 
          that if a bite by one of these three snakes requires antivenom 
          therapy, then Tiger Snake Antivenom is the preferred choice, not 
          Black Snake Antivenom. 
          Antivenom must be given intravenously.
          Since skin testing is unreliable and hazardous, there is no place 
          for pre-treatment sensitivity testing of antivenom.  (Sutherland 
          1983b; White 1987d). 
          Acute allergic reactions up to and including potentially fatal 
          anaphylaxis may occur during antivenom therapy.  Precautions 
          should be taken to reduce the risk to the patient.  These 
                Only give antivenom if staff, drugs and equipment to treat 
                severe anaphylaxis, including intubation facilities are 
                available (preferably in an intensive care unit), unless in 
                extreme emergency. 
                Always have adrenaline drawn up ready to use.
                Always have a good reliable IV line inserted.
                Always maintain adequate monitoring of patient during and 
                after antivenom therapy, especially blood pressure. 
                Dilute antivenom (1:5 to 1:10) in IV carrier solution 
                (normal saline; dextrose or Hartmann's). 

                Give antivenom initially very slowly and increase rate of 
                admnistration if there is no reaction; try to give whole 
                dose over 15-20 minutes. 
          Premedication is proposed by some (Sutherland 1983b). Suggested 
          premedications are subcutaneous adrenaline and intravenous 
          antihistamine.  The author of this monograph does not routinely 
          use such premedication.  (White 1987d)  Antihistamine may make 
          the patient drowsy or irritable, and thus interfere with the
          ongoing assessment of envenomation, especially in children.
          Adrenaline is potentially hazardous, especially in older patients
          or those with coagulopathy, and as acute severe allergic 
          reactions may be delayed up to an hour or more, such
          premedication is of doubtful value.  A patient with known or 
          likely allergy to horse serum presents a special case, where 
          premedication as above, possibly with the addition of steroids,
          should be considered.  Similarly, a sole country medical
          practitioner managing a severe snakebite, where antivenom must be
          given before an aeromedical evacuation team can arrive, may well 
          consider premedication with subcutaneous adrenaline a worthwhile
          For bites by P. australis, P. butleri and  P. papuanus, in the 
          presence of moderate systemic envenomation (as defined in 9.3) 
          initially give one ampoule of Black Snake Antivenom   Follow up 
          with further ampoule(s) if progression of symptoms and signs, 
          (White 1983c; 1987 c,d). 
          In the presence of severe envenomation, initially give 2 ampoules 
          of antivenom, and be prepared to give more, as above. 
          There is no mandatory upper limit on antivenom dosage, but only 
          rarely will more than 4-5 ampoules be required 
          Antivenom may not be required even in the presence of envenoming 
          for bites by P. porphyriacus, P. colletti and P. guttatus, except 
          possibly in children or the infirm (see above). If antivenom 
          therapy is indicated, commence with one ampoule of Tiger Snake 
          Antivenom. Only rarely would further doses be required. 
          10.6.2 Children
          The dosage of antivenom is identical in children to that in 
          adults.  However, in small children fluid volume considerations 
          may indicate the need for lower dilutions of antivenom.  For any 
          given bite the degree of envenomation will be worse in children 
          due to their lower body mass. 
          Following antivenom therapy there is a possibility that the 
          patient may develop serum sickness.  This should be explained to 
          the patient so that if symptoms develop, they will seek 
          appropriate treatment. 
          If large volumes of antivenom are used (eg 50-100 ml or more) 
          then prophylaxis for serum sickness should be considered (eg oral 

          steroid therapy for 2 weeks). 

     10.7 Management discussion

          Controversies in management exist in several areas, and have 
          already been discussed. 
          First aid
          Tourniquet versus pressure/immobilisation:  the latter is now 
          well accepted as the method of choice.  (Balmain & McClelland 
          1982, Fisher 1982, Murrell 1981, Sutherland 1983b; Sutherland et 
          al 1981 a,b; White 1987d) 
          Suction of wound:  No proven value.
          Cutting or excising wound:  of no practical value and potentially 
          Use of premedication:  not universally accepted.  (Sutherland 
          1975, 1977 a,b,c; 1983b; White 1987d) 
          Use of skin pretesting:  not appropriate.
          There are many aspects of Pseudechis venom worthy of further 
          research, at a basic science level, as well as studies at a more 
          clinical level. 


     11.1 Case reports from literature

          Case 1 (Rowlands et al, 1967)Pseudechis australis
          Fatal case of mulga snake bite in a 20 year-old man in Western 
          Australia. This is the only reported fatality from this species. 
          Bitten on the hand at least twice by a 1.8m specimen (positive 
          identification). At 2 hrs post-bite there was nausea and 
          vomiting. At 4 hrs post-bite he was lethargic with weak limb 
          movements, dilated but reactive pupils, and red urine (? 
          myoglobin). Given antivenom (no black snake antivenom available, 
          ie no specific antivenom therapy). Continued to deteriorate and 
          at 37 hrs post-bite was irritable, restless, drowsy, had 
          abdominal pain, little movement of upper part of chest, bilateral 
          ptosis, limited jaw movement, limited tongue extension, weak 
          skeletal muscle, decreased tendon jerks, and severe swelling of 
          the bitten hand and arm up to the axilla. The urine was still 
          red, and the plasma potassium raised (6.0 mEq/l). there was no 
          coagulopathy, but there was a thrombocytopenia (19 x 109/l). He 
          rapidly developed a progressive hypotension and then a fatal 
          cardiac arrest 39 hrs post-bite. Autopsy performed shortly after 
          showed severe subcutaneous oedema, haemorrhage and infiltration 

          with neutrophils at the bite site, two small subepicardial 
          haemorrhages, many small foci of swollen damaged myocardial 
          fibres, congested lungs with pulmonary oedema, congested swollen 
          kidneys, severe liver congestion, no specific brain abnormality 
          apart from congestion, and all sectioned skeletal muscle showed 
          swelling and acute coagulative necrosis of muscle fibres 
          consistent with rhabdomyolysis, worse in the muscles of the 
          bitten arm, the respiratory muscles, and the extra-ocular 
          Case 2      (Sutherland 1983)P. australis
          A 4 year-old girl was multiply bitten by a 1.8 m mulga snake on 
          the lower leg. By 15 mins post-bite she was pale, tachycardia 
          (160 bpm), vomiting, and had enlarged lymph nodes in her groin. 
          By about 45 mins post-bite she was semi conscious and had ptosis 
          and required respiratory support with oxygen. She was promptly 
          given polyvalent antivenom (2 amps), and thereafter made a rapid 
          improvement. There was no other evidence of a paralytic process, 
          nor a bleeding diathesis, and urine was normal. She subsequently 
          developed an abscess at the bite site. 
          Case 3      (Balmain & McClelland, 1982)P. australis
          A 3 year-old boy was bitten on the arm by a snake (later 
          positively identified as venom of mulga snake). By 20 mins he was 
          vomiting, but by 2 hrs he was conscious and in no distress 
          (effective first aid still in place), and had no evidence of 
          significant envenomation. Therefore no antivenom was given at 
          this time. He remained well until 20 hrs post-bite when he 
          developed "haematuria", at which time it was discovered he had 
          elevated FDP (> 40mg/l), prolonged clotting time (APTT 50 secs.). 
          A decision was made to give antivenom after review of the 
          results, commencing at about 26 hrs. post-bite. Subsequent 
          results showed myolysis (CPK 27500 U/l) and haemolysis (Hb fell 
          from 122 to 94 g/l). He subsequently made a complete recovery, 
          and did not develop renal failure. 
          Case 4      (Vines, 1978; White, 1981)P. australis
          A 24 year-old man was bitten on the thenar eminence by a large 
          mulga snake he was attempting to catch. He used a tourniquet as 
          first aid, and developed severe local swelling and subsequent 
          gangrene of the thumb requiring amputation. Prior to antivenom 
          therapy he had a prolonged clotting time, rectified after 
          antivenom. There was no evidence of neurotoxic problems, and no 
          details about the coagulopathy, or about evidence for myolysis or 
          renal damage. 
          Case 5 (Campbell, 1967)P. papuanus
          A report of experience with snakebite in Port Moresby, Papua New 
          Guinea with reference to bites by the Papuan black snake. 13 

          cases are listed, but subsequent experience suggests many or most 
          of these cases, where the snake was not positively identified, 
          were more likely due to other species (especially Oxyuranus 
          scutellatus canni). In only one case was the snake positively 
          identified. Overall, the series showed 9 of 13 cases with 
          paralysis (5 severe), 4 with coagulopathy, 4 with severe 
          haemolysis, and 1 with renal failure. 
          Case 6      (Sutherland, 1983)P. porphyriacus
          A brief review of 5 cases:
          (i)   15 year-old male bitten on the finger. Developed local 
          swelling and axillary tenderness, vomiting, and headache; 
          required antivenom therapy (6000 U Blacksnake antivenom). 
          Recovery uneventful. 
          (ii)  23 year-old male bitten on the foot. Developed local pain, 
          groin pain, but no systemic symptoms, possibly due to early 
          antivenom therapy (9000 U Blacksnake antivenom). 
          (iii) 7 year-old boy bitten on the foot. Developed local pain, 
          swelling, and vomiting and severe abdominal pain. Given 
          antivenom therapy (6000 U Blacksnake antivenom). Foot still 
          swollen the next day. 
          (iv)  23 year-old male bitten on the hand (?). Rapidly developed 
          vomiting, painful bitten arm and axilla, then abdominal 
          pain, blood-stained diarrhoea, and by 3 hrs post-bite 
          twitching of the limbs, mild headache, haematuria, and 
          faecal incontinence. Subsequent antivenom therapy (6000 U 
          Blacksnake antivenom) resolved his symptoms. 
          (v)   20 year-old male bitten on the finger. Developed local pain 
          and swelling, vomiting, latterly blood stained. antivenom 
          therapy was therefore given (6000 U Blacksnake antivenom), 
          with rapid recovery. 
          Case 7      (Sutherland, 1979)P. porphyriacus
          Very brief second hand report of a presumed bite by this snake 
          which resulted in grand mal convulsions in a previously well non-
          epileptic person. Outcome unknown. 
          Case 8      (Potter & Gaudry, 1988)P. porphyriacus
          A 24 year-old male was bitten on the hand. He used a tourniquet 
          as first aid. He developed severe pain in the bitten arm, 
          abdominal pain, nausea, vomiting, tender axillary adenopathy, and 
          there was no evidence of coagulopathy (tests NAD), or myolysis 
          (CPK 340 U/l). He was given antivenom therapy (3000 U Tiger snake 
          antivenom), and his symptoms resolved apart from severe pain in 
          the bitten arm and adjacent axilla, and a rise in CPK (to 1460 
          U/l on day 4). This settled over the next few days. It was 
          considered the severe arm pain was due to compartmental syndrome 
          secondary to local ischaemia caused by the tourniquet. 

     11.2 Internally extracted data on cases

       Mulga Snake bites (P. australis)

       Experience with 10 cases has been that most occurred in reptile 
       keepers or persons trying to catch snakes (7 of 10). 7 showed 
       some evidence of envenomation, mostly mild. No cases showed 
       paralytic symptoms or signs, or renal damage. In 3 cases there 
       was some evidence of a mild disturbance of coagulation, without 
       evidence of significant defibrination. In 4 cases there was 
       evidence of myolysis. All cases with significant envenomation 
       showed obvious local swelling, often involving much of the bitten 
       limb, and most bites were locally painful. 

       Case 1      (White, 1987d)P. australis

       A 48 year-old man in a remote country area was found unconscious 
       by his son and taken to the local hospital where he was noted as 
       drowsy, cold, hypotensive (BP 90/65), and with a swollen hand. 
       Later questioning revealed that at no time had the patient either 
       seen a snake or felt a bite. As he had a past history of 
       myocardial infarction a further episode was assumed. However 
       serial ECG and enzyme studies were not consistent with such  a 
       diagnosis, and the swollen hand and a peak CPK of 13758 U/l 
       suggested snakebite. Urine was positive for mulga snake venom. As 
       he was already recovering well no antivenom was given. 

       Case 2      (White, 1987d)P. australis

       An 11 year-old boy was bitten  on the thumb by a small (? 0.9m) 
       mulga snake he was trying to capture. He rapidly developed 
       headache, abdominal pain, nausea, vomiting, and local swelling 
       and pain in the bitten hand. He was given antivenom therapy    (1 
       amp. polyvalent antivenom, then 1 amp. blacksnake antivenom). He 
       remained drowsy overnight but then made a full recovery, apart 
       from the bitten hand which remained swollen  and painful for 
       several days. There was no evidence of paralytic problems, 
       significant coagulopathy (mild elevation of FDP), or renal 
       damage, and peak CPK was only 400 U/l. 

       Case 3 (White, unpublished case)P. australis

       A 17 year-old male was bitten on the hand  by a moderate sized 
       (approx 1.5-2 m) mulga snake he was trying to catch. He 
       subsequently developed headache, nausea, vomiting, diarrhoea, 
       dark urine, generalised aches and a painful swollen bitten hand. 
       As he was in a remote area retrieval and antivenom therapy were 
       delayed. By the time he was seen by the author he had a 
       significantly swollen tender hand, tender axilla, muscle movement 
       pain, reduced muscle power, but no ptosis, diplopia or other 
       evidence of classic paralytic envenomation. His urine was dark 
       red brown and positive for myoglobin. His peak CPK on day 2 was 
       25658 U/l. His renal function was normal, and FDPs were not 
       elevated although initially he had a slightly prolonged clotting 
       time (PR 1.4, APTT 49 secs). His urine remained dark for several 
       days, and his hand remained swollen and painful for about one 

       Red Bellied Black Snake bites (P. porphyriacus)

       Experience with 20 cases has been that while most show evidence 
       of envenomation (15 of 20), it is rarely more than mild and is 
       without significant complications. The only serious case was in a 
       reptile keeper previously bitten who had a severe anaphylactic-
       type reaction on a subsequent bite, with collapse, hypotension, 
       disseminated intravascular coagulation (DIC) and other secondary 
       problems. In most cases there was at least mild local pain and 
       swelling of the bite area, often associated with mild general 
       symptoms such as headache, abdominal pain, and nausea. None of 
       the cases showed evidence of paralysis, coagulopathy (compare 
       with above noted case with secondary DIC), myolysis or renal 

       Case 4      (White, 1987d)P. porphyriacus

       A 24 year-old male was bitten on his finger by his pet snake. He 
       had been consuming alcohol prior to the accident. About 1 hr 
       post-bite he became dizzy, short of breath, vomited, then lapsed 
       into unconsciousness for a brief period. At this time the bitten 
       hand was painful and swollen. Testing at this time did show any 
       evidence of coagulopathy or myolysis, and as he was 
       symptomatically improving and had a history of past antivenom 
       exposure no antivenom was used. He made a rapid recovery although 
       the hand remained swollen and painful for several days. 

       Case 5      (White, 1987d)P. porphyriacus

       A 9 year-old boy was bitten on his toe by an adult black snake 
       while walking near a creek. By 30 mins post-bite he was nauseous, 
  with abdominal pain, and shortly afterwards started vomiting. The 
  identity of the snake was confirmed by venom detection. Tests 
  showed no myolysis or significant coagulopathy (mild prolongation 
  of clotting time, ie PR 1.45). At 2 hrs post-bite he was 
  symptomatically improved and antivenom was withheld. At 4 hrs 
  post-bite he again developed abdominal pain and vomiting lasting 
  2 hrs, thereafter not recurring. The bitten foot was painful for 
  about 6 hrs, and was swollen for several days. 

  Blue bellied black snake

  Case 6      (White, unpublished case)P. guttatus

  A 33 year-old male was bitten on his hand while handling his pet 
  blue bellied black snake. By 1 hr post-bite the hand was painful, 
  starting to swell, and he developed a headache, nausea, and 
  blurred vision. There was no objective evidence of paralytic 
  problems, but he was tender in the axilla. There was no evidence 
  of coagulopathy or myolysis, and his general symptoms rapidly 
  improved without antivenom therapy. However the hand and arm 
  became progressively more painful and swollen, and a cellulitis 
  or compartmental syndrome was considered though not proven. 
  Antibiotic therapy was commenced but the arm remained swollen and 
  painful for about a week, then after apparently improving there 
  was a return of local symptoms which again took several days to 


  Collett's snake

  Case 7      (White, unpublished case)P. colletti

  A 16 year-old male was bitten on the hand by 3 pet snakes, one 
  being a small colletts snake. He developed local pain and 
  swelling, and drowsiness, but was neurologically stable. These 
  latter symptoms resolved rapidly but the hand remained swollen 
  for several days. There was no evidence of coagulopathy. 

11.3 Internal cases


12.1 Availability of antidotes and antitoxins

  Specific black snake antivenom, tiger snake antivenom and venom 
  detection kits are available directly from the manufacturer, 
  Commonwealth Serum Laboratories, 45 Poplar Road,  Parkville,  
  Victoria  3052,  Australia (telephone: 03-3891911,  telex: AA 
  32789, Fax: 61-3-3891434). 

12.2 Specific preventative measures:

  Avoid exposure to black snakes.  If working in areas where these 
  snakes exist, be alert, wear appropriate footwear and clothing, 
  do not place hands or other parts of body in places where snakes 
  may be present (eg down holes, in rubbish etc).  If handling or 
  catching snakes use appropriate techniques and equipment, 
  regularly checked to ensure peak performance, carry first aid 
  equipment (eg bandages, splint), never work alone, and have an 
  emergency plan documented and tested.  If allergy history or 
  known allergy to horse serum ensure this is documented 

12.3 Other

  No data available.


13.1 Clinical and Toxicological

  Balmain R & McClelland KL (1982)  Pantyhose compression bandage; 
  first aid measure for snakebite.  Med. J. Aust., 2:  240-241. 

  Barnes JM & Trueta J  (1941)  Absorption of bacteria toxins  and 
  snake  venoms  from  the  tissues:    importance  of  the  
  lymphatic circulation. Lancet, 1:  623-626. 

  Bernheimer AW, Weinstein SA, Linder R (1986)  Isoelectric 
  analysis of some Australian elapid snake venoms with special 
  reference to phospholipase B and haemolysis.  Toxicon  24(8):  

  Bernheimer AW, Linder R, Weinstein SA, Kim KS (1987)  Isolation 
  and characterization of a phospholipase B from venom of Collett's 
  snake Pseudechis colletti.  Toxicon  25(5):  547-554. 

  Broad AJ, Sutherland SK & Coulter AR (1979)   The lethality in 
  mice of dangerous Australian and other snake venoms.  Toxicon, 
  17: 661-664. 

  Campbell CH (1967)  The Papuan black snake (Pseudechis papuanus) 
  and the effect of its bite.  Papua New Guinea Med. J.  10(4):  

  Campbell CH, Chesterman CN (1972)  The effect of the venom of the 
  Papuan black snake (Pseudechis papuanus) on blood coagulation.  
  Papua New Guinea Med J..  15(3);   149-154. 

  Chandler, HM & Hurrell  JGR (1982)   A new  enzyme immunoassay 
  system suitable for  field use and  its application in  a snake 
  venom detection kit.  Clinica Chimica Acta, 121:  225-230. 

  Coulter AR, Sutherland SK & Broad AJ (1974) Assay of snake venoms 
  in tissue  fluids.  Journal of Immunological Methods, 4:297-300. 

  Coulter AR, Cox JC, Sutherland SK & Waddell CJ (1978)  A new  
  solid phase sandwich radioimmunoassay and its application to the 
  detection  of snake  venom.   Journal of Immunological Methods, 

  Coulter  AR,  Harris  RD  &  Sutherland  SK  (1980)   Enzyme 
  immunoassay  for the  rapid clinical  identification of  snake 
  venom.  Med. J. Aust., 1:  433-435. 

  Cull-Candy SG, Fohlman J,  Gustavsson D, Lullmann-Rauch R & 
  Thesleff S (1976)  The effects  of  taipoxin  and  notexin  on  
  the function and  fine structure  of the murine neuromuscular 
  junction.  Neuroscience, 1: 175-180. 

  Doery HM, Pearson JE  (1961)   Haemolysins in venoms of 
  Australian snakes.  Biochem. J.,  78:  820-27. 

  Dowdall MH,  Fohlman J & Eaker D (1977)   Inhibition of high 
  affinity choline  transport  in  peripheral  cholinergic  endings  
  by presynaptic snake venom neurotoxins.  Nature, 269:  700-702. 

  Eaker C (1978)  Studies of presynaptically neurotoxic and  
  myotoxic phospholipases A2.  In LI, C.H. Ed. Versatility of 
  Proteins, Academic Press. 

  Fairley NH (1929)a  The present position of snakebite and the 
  snake bitten in Australia.  Med. J. Aust., 1:  296-313. 

  Fairley  NH  (1929)b   The   dentition  and  biting  mechanism   
  of Australian snakes.  Med. J. Aust., 1:  313-327. 

  Fairley  NH & SPLATT B (1929)   Venom  yields  in Australian 

  poisonous snakes.  Med. J. Aust., 1:  336-348. 

  Fisher M (1982)  First aid in envenomation.  Med. J. Aust., 

  Harris JB, Johnson MA, Karlsson E (1975) Pathological responses 
  of rat skeletal muscle to a single subcutaneous injection of a 
  toxin isolated from the venom of the Australian tiger snake, 
  (Notechis scutatus  scutatus). Clin. exp. Pharm. Physiol. 2: 383-

  Hurrell JGR & Chandler HW (1982)  Capillary enzyme immunoassay 
  field kits for the detection of snake venom in clinical 
  specimens:  a review of two years' use.  Med. J. Aust., 2:  236-

  Leonardi TM, Howden MEH, Spence I,  (1979)  A lethal myotoxin 
  isolated from the venom of the Australian king brown snake 
  (Pseudechis australis).  Toxicon  17:  549-55. 

  Marshall LR, Herrmann RP (1983)  Coagulant and anticoagulant 
  action of Australian snake venoms.  Thrombosis Haemostasis 
  (Stuttgart), 50(3):707-711. 

  Marshall LR, Herrmann RP  (1989)  Australian snake venoms and 
  their in vitro effect on human platelets.  Thrombosis Research  

  Mebs D, Samejima Y  (1980)  Myotoxic phospholipases A from snake 
  venom, Pseudechis colletti, producing myoglobinuria in mice.  
  Experientia,  36:868-869. 

  Mebs D, Samejima Y (1980)  Purification from Australian elapid 
  venoms and properties of phospholipases A which cause 
  myoglobinuria in mice. Toxicon,  18:  443-454. 

  Mebs D, Ehrenfeld M, Samejima Y (1983)  Local necrotizing effect 
  of snake venoms on skin and muscle: relationship to serum 
  creatine kinase. Toxicon,  21(3):393-404. 

  Moon KE, Rys A (1984)  Amino terminal analysis of Pseudexin from 
  the venom of the Australian red-bellied black snake (Pseudechis 
  porphyriacus). Toxicon  22(1):  165-167. 

  Murrell G (1981) The effectiveness of the pressure/immobilization    
  first aid technique  in the  case of a tiger  snake bite.   Med. 
  J. Aust., 2:  295. 

  Nishida S, Terashima M, Shimazu T, Takasaki C, Tamiya N  (1985a) 
  Isolation and properties of two phospholipases A2 from the venom 
  of an Australian elapid snake (Pseudechis australis).  Toxicon  

  Nishida S, Terashima M, Tamiya N  (1985b)  Amino acid sequences 
  of phospholipases A2 from the venom of an Australian elapid snake 
  (Pseudechis australis).  Toxicon  23:  87-104. 

  Potter D, Gaudry P (1988)  A case of snakebite with unusual 
  features. Med. J. Aust.,  149:  565. 

  Rowan EG, Harvey AL, Takasaki C, Tamiya N (1989)  Neuromuscular 
  effects of three phospholipases A2 from the venom of the 
  Australian king brown snake Pseudechis australis.  Toxicon.  27:  

  Rowlands JB, Mastaglia FL, Kakulas BA, Hainsworth DA (1969)  
  Clinical and pathological aspects of a fatal case of mulga 
  (Pseudechis australis) snakebite.  Med. J. Aust.  1:  226-229. 

  Schmidt JJ, Middlebrook JL (1989)  Purification sequencing and 
  characterization of Pseudexin phospholipases A2 from Pseudechis 
  porphyriacus (Australian red-bellied black snake).  Toxicon  

  Sutherland SK (1974)   Venomous Australian creatures:  the action 
  of their toxins and the care of the envenomated patient.  
  Anaesthesia and Intensive Care, 2(4):316-327. 

  Sutherland SK (1975) Treatment of snakebite in Australia:  some 
  observations and recommendations.  Med. J. Aust., 1:30-32. 

  Sutherland SK (1977)a  Serum reactions:  an analysis of  
  commercial antivenoms  and the  possible role  of 
  anticomplementary  activity in de-novo reactions to  antivenoms 
  and antitoxins.  Med. J. Aust.,  1: 613-615. 

  Sutherland SK (1977)b  Antivenoms:  better late than never.   
  Med. J. Aust., 2:813. 

  Sutherland SK (1977c)   Acute  untoward  reactions to antivenoms.  
  Med. J. Aust., 1:841. 

  Sutherland SK (1979)   Epilepsy after envenomation by a red-
  bellied black snake.   Med. J. Aust.   2:257. 

  Sutherland SK (1981)  When do  you remove first aid measures  
  from an envenomed limb.  Med. J. Aust., 1:542-543. 

  Sutherland SK (1983)   Prolonged  use of pressure/immobilization 
  after snake bite.  Med. J. Aust., 1:  58. 

  Sutherland SK (1983)  Australian Animal Toxins, Melbourne,  
  Oxford University Press. 

  Sutherland SK, Campbell DG & Stubbs AE (1981)  A  study of the 
  major Australian snake venoms in the monkey (Macaca 
  fascicularis), II:  myolytic and haematological effects of 
  venoms.  Pathology, 13:  705-715. 

  Sutherland SK, Coulter AR, Broad AJ, Hilton JMN &  Lane LHD  
  (1975) Human snakebite victims:  the successful detection of 
  circulating  snake venom  by  radioimmunoassay.   Med.  J. Aust., 


  Sutherland SK & Coulter AR (1977) Three instructive cases of 
  tiger snake (Notechis scutatus) envenomation, and how a 
  radioimmunoassay proved the diagnosis.  Med. J. Aust., 2:  177-

  Sutherland SK &  Coulter AR (1977)  Snake bite:  detection  of 
  venom by radioimmunoassay.  Med. J. Aust., 2:  683-684. 

  Sutherland SK,  Coulter AR  &  Harris  RD (1979) Rationalisation  
  of first-aid measures for elapid snakebite.  Lancet, 183-186. 

  Sutherland SK,  Coulter  AR,  Harris  RD,  Lovering KE & Roberts 
  ID (1981)  A study of the major Australian snake venoms in the  
  monkey (Macaca  fascicularis);  in  the  movement  of  injected 
  venom; methods which retard  this movement,  and the  response to 
  antivenoms.  Pathology, 13:  13-27. 

  Sutherland SK &  Lovering  KE (1979)   Antivenoms:   use and 
  adverse reactions  over a 12 month period  in Australia and Papua 
  New Guinea. Med. J. Aust., 2:  671-674. 

  Takasaki C,  Tamiya N (1982)  Isolation and properties of 
  lysophospholipases from the venom of the Australian elapid snake 
  Pseudechis australis.  Biochem J.  203:  269-276. 

  Takasaki C, Tamiya N (1985)  Isolation and amino acid sequence of 
  a short chain neurotoxin from an Australian elapid snake 
  Pseudechis australis.  Biochem. J.  232:  367-371. 

  Takasaki C (1989)  Amino acid sequence of a long chain neurotoxin 
  homologue Pa 1D from the venom of an Australian elapid snake 
  Pseudechis australis.  J. Biochem.  106:  11-16. 

  Takasaki C, Sugama A, Yanagita A, Tamiya N, Rowan EG, Harvey AL 
  (1990a)  Effects of chemical modifications of Pa-11 a 
  phospholipase A2 from the venom of the Australian king brown 
  snake (Pseudechis australis) on its biological activities.  
  Toxicon  28(1):  107-117. 

  Takasaki C, Suzuki J, Tamiya N (1990b)  Purification and 
  properties of several phospholipases A2 from the venom of 
  Australian king brown snake (Pseudechis australis).  Toxicon.  
  28(3):  319-327. 

  Takasaki C, Yutani F, Kajiyashiki T,  (1990c)  Amino acid 
  sequence of eight phospholipases A2 from the venom of Australian 
  king brown snake Pseudechis australis.  Toxicon  28(3):  329-339. 

  Trethewie ER (1971)  The pharmacology and toxicity of the venoms 
  of the snakes of Australia and Oceania. In Eds.  Bucherl W, 
  Buckley EE, Venomous Animals And Their Venoms,  Academic Press, 
  New York, : 79-101. 

  Trinca JC (1963)  The treatment  of snakebite.  Med. J. Aust.,  


  Vaughan GT, Sculley TB, Tirrell R (1981)  Isolation of a toxic 
  phospholipase from the venom of the Australian red-bellied black 
  snake (Pseudechis porphyriacus)  Toxicon  19:  95-101. 

  Vines A (1978)  Severe local reaction to bite of king brown 
  snake.  Med. J. Aust.  1:657. 

  White J (1981)   Ophidian   envenomation;  a   South  Australian 
  perspective.  Records of  the  Adelaide  Children's  Hospital,  
  2(3): 311-421. 

  White J (1983)a   Patterns of elapid  envenomation and treatment  
  in South Australia.  Toxicon, Suppl. 3:  489-491. 

  White J (1983)b   Local tissue destruction and Australian elapid 
  envenomation.  Toxicon, Suppl. 3:  493-496. 

  White J (1983)c  Haematological problems and Australian elapid 
  envenomation.  Toxicon, Suppl. 3:  497-500. 

  White J (1987)a  Elapid   snakes:   venom  production  and   bite 
  mechanism.  In Covacevich, J., Davie, P. & Pearn, J. Eds.  Toxic 
  Plants & Animals:  a guide for Australia, Queensland Museum, 504 

  White J (1987)b  Elapid  snakes:  venom toxicity and  actions.  
  In Covacevich J, Davie P & Pearn J Eds. Toxic Plants & Animals:  
  a guide for Australia, Queensland Museum, 504 pp. 

  White J (1987)c Elapid snakes:  aspects of envenomation.  In 
  Covacevich J, Davie P & Pearn J Eds. Toxic Plants & Animals:  a 
  guide for Australia, Queensland Museum, 504 pp. 

  White J (1987)d  Elapid   snakes:   management   of  bites.   In 
  Covacevich J, Davie P & Pearn J Eds. Toxic Plants & Animals:  a 
  guide for Australia, Queensland Museum, 504 pp. 

13.2 Zoological

  Cogger HG (1971)  The venomous snakes of Australia and Melanesia.  
  In Eds. Bucherl, W., Buckley, E.E.,  Venomous Animals And Their 
  Venoms, Academic Press, New York,: 35-77. 

  Cogger HG (1975) Reptiles  and Amphibians  of Australia, Sydney, 
  A.H. & A.W. Reed. 

  Cogger HG (1987)   The venomous land  snakes.  In Covacevich J, 
  Davie P &  Pearn J  Eds. Toxic  Plants &  Animals:  a  guide for 
  Australia, Brisbane, Queensland Museum, 504 pp. 

  Cogger HG,  Cameron EE  &  Cogger HM (1983)   Zoological 
  catalogue of Australia,  Volume I,  Amphibia and  Reptilia, 
  Canberra, Australian Government Publishing Service. 

  Covacevich J (1988)  Australia's dangerous snakes.  In Pearn J  & 
  Covacevich J Eds. Venoms and Victims, Brisbane, Queensland 

  Longmore R (1986)  Atlas  of elapid snakes of  Australia, 
  Canberra, Australian Government Publishing Service. 

  Schwaner TD,  Baverstock  PR,  Dessauer HC & Mengden GA (1985) 
  Immunological evidence for the phylogenetic relationships of 
  Australian elapid snakes.  In Grigg, G., Shine, R. & Ehmann, H.  
  Eds. Biology  of Australasian Frogs  and Reptiles, New  South 
  Wales, Royal Zoological Society.


     Author:    Dr Julian White
                State Toxinology Services
                Adelaide Children's Hospital
                North Adelaide,  South Australia 5006

                Phone: 61-8-2047000
                Mobile phone: 61-18-832776
                Fax: 61-8-2046049

     Date:      August  1990

     Peer review:Singapore, November 1991.

    See Also:
       Toxicological Abbreviations